Decreased ENaC expression compensates the increased NCC activity following inactivation of the kidney-specific isoform of WNK1 and prevents hypertension. - Wikidata - thesis-toulmin - TriplyDB

Decreased ENaC expression compensates the increased NCC activity following inactivation of the kidney-specific isoform of WNK1 and prevents hypertension.

Decreased ENaC expression compensates the increased NCC activity following inactivation of the kidney-specific isoform of WNK1 and prevents hypertension.

http://www.wikidata.org/entity/Q34241490

about

Ubiquitylation and control of renal Na+ balance and blood pressure Epithelial sodium transport and its control by aldosterone: the story of our internal environment revisited A SPAK isoform switch modulates renal salt transport and blood pressure Emerging Targets of Diuretic Therapy.Mechanism of salt-sensitive hypertension: focus on adrenal and sympathetic nervous systems Renal tubular NEDD4-2 deficiency causes NCC-mediated salt-dependent hypertension The WNKs: atypical protein kinases with pleiotropic actions.The Cap1-claudin-4 regulatory pathway is important for renal chloride reabsorption and blood pressure regulation.Recent advances in distal tubular potassium handling Paradoxical activation of the sodium chloride cotransporter (NCC) without hypertension in kidney deficient in a regulatory subunit of Na,K-ATPase, FXYD2.Sodium reabsorption in the thick ascending limb in relation to blood pressure: a clinical perspective.WNK1 activates large-conductance Ca2+-activated K+ channels through modulation of ERK1/2 signaling.Overexpression of the sodium chloride cotransporter is not sufficient to cause familial hyperkalemic hypertension.The epithelial sodium channel γ-subunit gene and blood pressure: family based association, renal gene expression, and physiological analyses.Double knockout of pendrin and Na-Cl cotransporter (NCC) causes severe salt wasting, volume depletion, and renal failure Kidney-specific WNK1 inhibits sodium reabsorption in the cortical thick ascending limb Regulation of the renal Na+-Cl- cotransporter by phosphorylation and ubiquitylation.Kidney-specific WNK1 regulates sodium reabsorption and potassium secretion in mouse cortical collecting duct.Effects of ACE inhibition and ANG II stimulation on renal Na-Cl cotransporter distribution, phosphorylation, and membrane complex properties An unexpected journey: conceptual evolution of mechanoregulated potassium transport in the distal nephron.Overexpression of pendrin in intercalated cells produces chloride-sensitive hypertension.Hypertension: the missing WNKs.WNK1-related Familial Hyperkalemic Hypertension results from an increased expression of L-WNK1 specifically in the distal nephron.Regulation of BK-α expression in the distal nephron by aldosterone and urine pH.Enhanced phosphorylation of Na(+)-Cl- co-transporter in experimental metabolic syndrome: role of insulin.The WNK kinase network regulating sodium, potassium, and blood pressure.Exploring the intricate regulatory network controlling the thiazide-sensitive NaCl cotransporter (NCC).Independent regulation of Na+ and K+ balance by the kidney.The WNK-SPAK/OSR1 pathway: master regulator of cation-chloride cotransporters.Physiology and pathophysiology of the renal Na-K-2Cl cotransporter (NKCC2).Renal mechanisms of salt-sensitive hypertension: contribution of two steroid receptor-associated pathways.Dietary potassium and the renal control of salt balance and blood pressure.Revisiting the NaCl cotransporter regulation by with-no-lysine kinases.Relative roles of principal and intercalated cells in the regulation of sodium balance and blood pressure.ROMK expression remains unaltered in a mouse model of familial hyperkalemic hypertension caused by the CUL3Δ403-459 mutation.Pharmacological targeting of SPAK kinase in disorders of impaired epithelial transport.Modulation of NCC activity by low and high K(+) intake: insights into the signaling pathways involved.An inducible transgenic mouse model for familial hypertension with hyperkalaemia (Gordon's syndrome or pseudohypoaldosteronism type II).WNK3 abrogates the NEDD4-2-mediated inhibition of the renal Na+-Cl- cotransporter.Loss of WNK3 is compensated for by the WNK1/SPAK axis in the kidney of the mouse.

P2860

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P2860

Decreased ENaC expression compensates the increased NCC activity following inactivation of the kidney-specific isoform of WNK1 and prevents hypertension.

http://www.wikidata.org/entity/Q34241490

description

2010 nî lūn-bûn

@nan

2010 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

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2010 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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name

Decreased ENaC expression comp ...... NK1 and prevents hypertension.

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Decreased ENaC expression comp ...... NK1 and prevents hypertension.

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Decreased ENaC expression comp ...... NK1 and prevents hypertension.

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type

label

Decreased ENaC expression comp ...... NK1 and prevents hypertension.

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Decreased ENaC expression comp ...... NK1 and prevents hypertension.

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Decreased ENaC expression comp ...... NK1 and prevents hypertension.

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prefLabel

Decreased ENaC expression comp ...... NK1 and prevents hypertension.

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Decreased ENaC expression comp ...... NK1 and prevents hypertension.

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Decreased ENaC expression comp ...... NK1 and prevents hypertension.

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PNAS.1006128107

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Proceedings of the National Academy of Sciences of the United States of America

P1476

Decreased ENaC expression comp ...... NK1 and prevents hypertension.

@en

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Cara Büsst

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Christelle Soukaseum

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Jean-Luc Elghozi

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Johannes Loffing

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Juliette Hadchouel

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Michelle Cambillau

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Richard P Lifton

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Tany Zürrer

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Véronique Baudrie

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Xiao-ou Zhou

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P2860

WNK3 kinase is a positive regulator of NKCC2 and NCC, renal cation-Cl- cotransporters required for normal blood pressure homeostasis

The thiazide-sensitive Na-Cl cotransporter is regulated by a WNK kinase signaling complex

Antagonistic regulation of ROMK by long and kidney-specific WNK1 isoforms.

Molecular pathogenesis of inherited hypertension with hyperkalemia: the Na-Cl cotransporter is inhibited by wild-type but not mutant WNK4

Multiple promoters in the WNK1 gene: one controls expression of a kidney-specific kinase-defective isoform

WNK4 enhances the degradation of NCC through a sortilin-mediated lysosomal pathway

Regulation of ROMK channel and K+ homeostasis by kidney-specific WNK1 kinase

Human hypertension caused by mutations in WNK kinases

Activation of the thiazide-sensitive Na+-Cl- cotransporter by the WNK-regulated kinases SPAK and OSR1

WNK4 regulates the balance between renal NaCl reabsorption and K+ secretion

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18109-18114

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scholarly article

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10.1073/PNAS.1006128107

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42

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107

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Xavier Jeunemaitre

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2010-10-04T00:00:00Z

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47336599

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20921400

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